Chloroacetophenone (CN) Poisoning

 Materials and Methods

This presentation includes clinical data including testimony by expert witnesses indicating the characteristics of the space in which the individual was exposed, the hospital course and the necropsy findings. In addition, the clinical data, records, microscopic sections, photographic documentation or paraffin tissue blocks were requested from those forensic pathologists who had observed instances of death following exposure to tear-gas. The clinical history of each of these cases was briefly reviewed in conjunction with the available pathologic findings.

Clinical Review: A 29-year-old white single man (last employed as neighborhood newspaper delivery boy) was admitted to the emergency room of the Albany Medical Center Hospital on October 7, 1958. The home in which he and his mother lived had been condemned for removal in preparation for the development of a state superhighway. On several occasions, he became belligerent on contact with the contractors who were clearing the land surrounding his home. On the day of admission damage was caused to the motor vehicles of the contractor and he was suspected of having tossed rocks through the windshields of these vehicles. A state trooper, called to investigate this incident. While in the company of a physician, attempted to interrogate the subject but he began throwing tire jacks and chairs and barricaded himself in his room and loudly proclaimed he would not be taken alive. A single #112 tear gas grenade containing 128 grams. (Figs. 1 ~ 2) of chloroacetophenone gas was then fired into this room. Only a small high window which was raised slightly and one broken panel of a wooden door allowed for air exchange on n still day in a room 9'1" x 9'1" x 8'6". The patient was exposed to the gas in this room for approximately 30 minutes.

Family History: The patient had had an apparently normal childhood until the age of 17 when his father died. Following a car accident in which he ran off the road approximately 10 years ago, he became withdrawn and paranoid. During the past two years the patient had had periods of not taking care of himself.

Physical Examination: On admission to the hospital the patient was agitated and under restraints. His clothes and body smelled of tear gas. His temperature was 99°F.; pulse 80; respiration 24; blood pressure 130/80. The conjunctivae were suffused. The pupils were small and unreactive, There was abundant mucoid discharge from both the nose and the mouth, By auscultation the chest was clear. However, the heart had an irregular rhythm. The cardiogram was interpreted as within normal limits but with occasional premature ventricular contractions. The neurological examination was unremarkable except for the absence of the Babinski reflex.

He remained in a semicomatose condition for approximately 12 hours and then suddenly developed pulmonary edema and died.

Necropsy. Gross Descriptions: The body was that of an extremely well developed, moderately obese white male who looked older than the stated age of 29 years, He appeared older because his black hair, although receded centrally to the vertex, was in long unkempt locks peripherally and there was also a long unkempt beard. The face, neck and upper chest were intensely cyanotic, The conjunctivae were markedly suffused, and the pupils were 0.2 cm. in diameter, round and equal. The buccal mucous membranes were cyanotic. The tongue was pressed against the clenched jaws. The mouth and nasal passages exuded abundant frothy fluid. The chest showed some increase in the anterior-posterior diameter and the abdomen was moderately protuberant, The external genitalia were not remarkable, nor were the extremities. On the skin there were a few very superficial small abrasions not larger than 3 cm. in length and less than 0.5 cm. in width, on the left shoulder, right knee and in the mid-abdomen.

The body was completely rigid. There was also moderate postmortem dependent lividity. The linings of all the body cavities were smooth and no abnormal accumulations of fluid were present. Each lung weighed approximately 1,000 gm. The mucosa of the trachea and bronchi was tremendously swollen and covered by frothy pale fluid, On section of the lungs the pulmonary tissues showed extreme edema and in the basilar portions, particularly posteriorly, there were foci of intra-alveolar hemorrhage.

The organs of the neck including the tongue, larynx, trachea, and esophagus were removed en bloc. It was quite apparent that all of the respiratory tissues, starting from the mucosa of the pyriform sinus and including the intrinsic structures of the larynx and extending to the trachea, showed marked swelling and were covered with bubbly frothy fluid.

The stomach was moderately dilated and filled with about 200 ml. of thin yellowish fluid. Among the longitudinal furrows of the lesser curvature there were numbers of petechiae.

The brain weighed 1,600 gm. Although the leptomeninges were thin, an increase in fluid in the subarachnoid space was present. The cerebellar hemispheres showed early tonsillar herniation. The ventricular system was normal. The remainder of the organs were not remarkable grossly.

Microscopic Examination: Multiple sections from the larynx, trachea and bronchi showed diffuse superficial acute necrosis of the respiratory mucosa with the formation of a pseudomembrane of fresh fibrin mixed with acute inflammatory cells. The submucosal tissues were tremendously swollen due to congestion, edema, and acute inflammatory cell infiltration.

Many of the bronchioles showed desquamation of their lining epithelium and their walls were edematous and acutely inflamed. In some other regions the desquamated surface was covered by a fibrinous pseudomembrane. Occasionally the adjacent pulmonary arteries showed acute inflammation of their walls.

The alveolar capillaries were markedly congested and virtually all of the alveoli were filled with protein-rich fluid. In places, a hyaline membrane lined the alveoli. In other foci the presence of fluid mixed with blood and acute inflammatory cells was indicative of early bronchopneumonia.

A number of hepatic cells contained cytoplasmie fat vacuoles. Multiple sections from various levels of the brain showed moderate generalized congestion. In many areas there was evidence of perivascular edema and minute perivascular hemorrhages.

Review of available documents in other cases failed to indicate precise data such as name of the shell manufacturer, the amount of chemical in each shell, size of the room, the weather, etc. to allow for careful comparison with our case.

Discussion

The structural formula of chloroacetophenone is C6H5COCH2C1. When pure, it consists of colorless crystals, 1.3 specific gravity melting point 59°C., boiling point 247°C., yielding a vapor which in low concentrations has an odor resembling apple blossoms.

Although chloroacetophenone is classed as a lacrimator, in adequate concentrations it has many toxic effects beyond that of lacrimation. In toxic doses it is a severe irritant to the entire respiratory tree and ultimately the chemical injury facilitates the development of acute pulmonary edema and death. Other findings indicate that in certain concentration it will produce first and second degree burns of the skin. In addition there are secondary complications, possibly due to absorption of the chemical associated with accompanying anoxia. All subjects about which we have information were reported to be extremely agitated and there were evidences of neurological defects manifested by pinpoint pupils, semicoma loss of reflexes, and other findings. Some of the patients did show early hepatic fatty changes even though the total history from exposure to death was only a matter of a few hours.

An intolerable concentration is considered to be 0.0045 mg per liter: that is, 45 ten thousandth of an ounce in a thousand cubic feet. In a human being this will produce tearing, burning of the eyes and difficulty in breathing so that he will make every effort to leave. The estimated human lethal concentration for 10 minutes' exposure of chloroacetophenone is 0.85 mg. per liter, which is equivalent to 0.85 ounces per thousand cubic feet. In our case, the single grenade used contained 128 gm. which is equivalent to 4.5 ounces. Therefore, the agent was dispersed in a room 700 cubic feet, which is over 5 time the lethal concentration per thousand cubic feet.

In such calculations, the opening of doors or windows, insulation's of the walls, the character of the wind outside and many other factors permitting convection losses which would affect the concentration in the room, cannot be taken into account.

Since the gas has a higher specific gravity than air, it would tend to sink to the bottom of the room so that the dispersal effects of windows which had been opened from the top would he small.

Front previous experimental studies it is estimated that exposure to less than 1 ounce per thousand cubic feet for 10 minutes would he lethal (2). If the barricaded individual is in possessions of any lethal weapon, no risk should be entertained by the law enforcement officer. However, if not, after roughly calculating the exposure, an attempt to create air convection by breaking down the door or windows or even going in after the individual should be considered. Such aggressive corrective attempts are desirable because of the frequency with which psychotic individuals who have not committed a major crime are involved.

Summary

A 29 years old man barricaded in a small room was exposed to chloroacetophenone (CN tear gas) from a single #112 grenade for approximately 30 minutes. Thereafter he was subdued and brought to the hospital for therapy. He died in acute pulmonary edema 12 hours after admission. The pathology observed was described. Caution in the use of tear gas grenades should lie tempered by a number of factors including knowledge of the lethal exposure dose, the contents of the grenade, volume estimation of the physical enclosure, the mental status and the weapons available to the individual.

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